Catalpol from Rehmannia glutinosa Targets Nrf2/NF-[Formula: see text]B Signaling Pathway to Improve Renal Anemia and Fibrosis.

Rehmannia glutinosa is widely recognized as a prominent medicinal herb employed by practitioners across various generations for the purpose of fortifying kidney yin. Within Rehmannia glutinosa, the compound known as catalpol (CAT) holds significant importance as a bioactive constituent. However, the protective effects of CAT on kidneys, including ameliorative effects on chronic kidney disease - most prominently renal anemia and renal fibrosis - have not been clearly defined. In this study, the kidney injury model of NRK-52E cells and C57BL/6N male mice was prepared by exposure to aristolochic acid I (AA-I), and it was discovered that CAT could ameliorate oxidative stress injury, inflammatory injury, apoptosis, renal anemia, renal fibrosis, and other renal injuries both in vivo and in vitro. Further treatment of NRK-52E cells with Nrf2 inhibitors (ML385) and activators (ML334), as well as NF-[Formula: see text]B inhibitors (PDTC), validated CAT's ability to target Nrf2 activation. Furthermore, the expression of phosphorylated NF-[Formula: see text]B p65, IL-6, and Cleaved-Caspase3 protein was inhibited. CAT also inhibited NF-[Formula: see text]B, and then inhibited the expression of IL-6, p-STAS3, TGF-[Formula: see text]1 protein. Therefore, CAT can regulate Nrf2/NF-[Formula: see text]B signaling pathway, significantly correct renal anemia and renal fibrosis, and is conducive to the preservation of renal structure and function, thus achieving a protective effect on the kidneys.

Avermectin induced liver injury in pigeon: mechanisms of apoptosis and oxidative stress.

Extensive use of avermectin (AVM) can result in environment pollution, and it is important to evaluate the potential impact this antibiotic has on ecological systems. Few published literatures have discussed the liver injury mechanisms induced by AVM on birds. In this study, pigeons were exposed to feed containing AVM (0, 20, 40 and 60 mg/kg diet) for 30, 60, 90 days respectively. The results showed that AVM increased the number of apoptosis and the expression level of caspase-3, 8, fas mRNA in the liver of pigeons. Ultrastructural alterations, including mitochondrial damage and chromatin aggregation, become severe with increase exposure dose. Exposure to AVM induced significant changes in antioxidant enzyme {superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)} activities and malondialdehyde (MDA) content, augmented protein carbonyl (PCO) content and DNA-protein crosslink (DPC) coefficient, in a concentration-dependent manner in the liver of pigeons. Our results show that AVM has toxic effect in pigeon liver, and the mechanism of injury caused by AVM is closely related to apoptosis and oxidative stress.

Cadmium-induced injury and the ameliorative effects of selenium on chicken splenic lymphocytes: mechanisms of oxidative stress and apoptosis.

Cadmium (Cd) is an important environmental pollutant present in soil, water, air, and food. Selenium (Se) can antagonize some metal element toxicity including Cd. To investigate the cytotoxicity of Cd and the protective effects of Se on bird immunocytes in vitro, chicken splenic lymphocytes with CdCl2 (10(-6) mol/L), Na2SeO3 (10(-7) mol/L), and the mixture (10(-7) mol/L Na2SeO3 and 10(-6) mol/L CdCI2) were incubated for 12, 24, 36, and 48 h, respectively. A high level of malondialdehyde (MDA) and reactive oxygen species (ROS) productions were observed in Cd treatment group; the activities of catalase (CAT), glutathione peroxidise (GSH-Px), superoxide dismutase (SOD), and the mitochondrial inner transmembrane potential (ΔΨm) were significantly lower in Cd treatment group than those in controls (P < 0.05 or P < 0.01). In contrast, Se significantly improved the activities of antioxidant enzymes and reduced MDA and ROS levels compared to Cd treatment alone group, although not restored to the levels of control group. The population of apoptosis cells demonstrated that Cd induces the apoptosis of chicken splenic lymphocytes; in addition, increased mRNA level of Bak, p53, caspase-3, caspase-9, and cytochrome c (Cyt c) and decreased Bcl-2, Bcl-xl, and CaM were observed in Cd treatment group. Se ameliorated ΔΨm and [Ca(2+)]i for mitochondria function restoring, and Se was able to modulate the expression of relative genes. In conclusion, concurrent treatment with Se reduced the Cd-induced morphological changes and oxidative stress, ion disorder, and apoptosis, suggesting that the toxic effects of Cd on the chicken splenic lymphocytes were partly meliorated by Se.

Effects of avermectin on heat shock proteins expression and histopathology in spleen tissues of pigeon.

Avermectin (AVM) is the active component of some insecticidal and nematicidal product used in agriculture and veterinary medicine for the prevention of parasitic diseases. Residues of AVM in environment have toxic effects on non-target aquatic and terrestrial organisms. Heat shock proteins (Hsps) are commonly used by environmental toxicologists as biochemical markers of exposure to various chemical and other stressors. The objective of this study was to investigate whether sub-chronic AVM exposure would alter the levels of stress proteins, Hsps in the pigeon spleen after 30, 60 and 90days. Our results showed that Hsp60, Hsp70 and Hsp90, and their corresponding messenger RNA (mRNA) transcriptions (as well as Hsp30) significantly elevated, meanwhile, obviously histopathological changes were not observed in pigeons spleens after early AVM exposure. Then the expression of Hsps relatively decreased and obvious histopathological damages occurred in the spleen tissues with continued AVM exposure. So we suggest that the elevations of Hsps can be as a part of protective mechanism to reduce cellular damage, and important markers to help assess the toxicity induced by AVM. The reduction of Hsps in spleen implies that the tissues are damaged by long-term and excessive AVM exposure. Thus, the information presented in this study is believed to be helpful in supplementing data for further AVM toxicity study.